THE ROLE OF T REGULATORY AND TH17 CELLS IN THE PATHOGENESIS OF RHEUMATOID ARTHRITIS (REVIEW).

Chronic inflammation of joints of autoimmune origin - rheumatoid arthritis - develops due to deplorable coincidence of genetic, immune and environmental factors. Th17 cells are considered as the main effector cells in the pathogenesis of rheumatoid arthritis. Analysis of many reports clarify positive correlation between the frequencies of circulating Th17 cells, serum levels of IL-17A and IL-23, synovial IL-17 and disease activity. Autoreactive Th clone response is regulated by the certain population of suppressor cells - T regulatory cells (Tregs). Contradictory results have been reported concerning Treg cell proportion in RA peripheral blood, but there is a general agreement on Treg cell enrichment in RA synovial fluid, that somehow compensates inflammation, but cytokine environment in the inflamed joint reduces functional activity of Tregs. Imbalance between Th17 and Treg cells may play a initiative role in RA pathogenesis because predominant Th17 cells can provoke vigorous pro-inflammatory response by producing IL-17 and impaired Tregs, partly due to the cytokine microenvironment, cannot regulate autoreactive immune response. Currently, a major focus of study in RA is to control IL-17 and modulate Treg activity in order to design new and improved therapies to limit inflammation and re-establish self-tolerance.